Test 3 Flashcards
(198 cards)
1
Q
What is normal flora
A
Mircroorganisms that live in or on your body
2
Q
What parts of the body are microorganisms found in (in general)
A
Tracts (parts that lead to the outside of the body
3
Q
Resident flora
A
Microorganisms found at a given site at a host’s particular age
4
Q
Transient flora
A
Microorganism that live on the body for a short period of time
- shouldnt stay too long
- okay as long as the resident flora remain intact
5
Q
What happens when the resident flora decreased
A
The trasient increases and makes you sick
6
Q
What types of microorganisms are normal flora
A
Usually bacteria. Some people have protozoa and fungi
7
Q
Where are microorganisms mostly found of the body
A
Skin and mucus
8
Q
Comensil
A
Benefits from its association with you. You get nothing and you are not harmed
9
Q
Mutualistic
A
You and the microorganism benefit from the association
10
Q
Opportunistic pathogens
A
Cause disease when your immune system is compromised or tissue damage
11
Q
Primary pathogens
A
Make healthy people sick
12
Q
Origin of normal flora
A
Fetus is germ free. As the fetus moves through the birth canal, microorganisms attach. They also attach from breathing and eating
13
Q
What did pasteur do
A
Raised germ free animals (chickens in incubator). Chick was normal. Life is possible without microorganisms
14
Q
What did reineir do
A
Raised germ free animals (gnomobiotic) rats and chicks. Exposed one or two microorganisms to them. Immune system was underdeveloped and they were vulnerable to pathogenic and nonpathogenic organisms
15
Q
Effect antibiotics have on the normal flora
A
- Suppress normal flora
- Other microorganisms become opportunistic and cause disease
- Normal flora suppresses opportunistic pathogens
16
Q
Characteristics of normal flora
A
- Adherence to host cells
- Can produce antimicrobial substances
17
Q
How do the normal flora adhere to host cells
A
Proteins or polysaccharides make them sticky
Pili
18
Q
Desquamation
A
Process in which body cells shed off. Any bacteria attached to them comes off with it (defense mechanism)
19
Q
What do the normal flora produce antimiicrobial substances
A
Prevent other microorganisms from attachting (no competition)
20
Q
Should the blood, body fluids and tissues have microorganisms
A
No
21
Q
How do microorganisms get into the blood, blody fluids and tissues. What results
A
They enter through cuts into the blood and to the heart (endocarditis)
22
Q
What is the first line of defense
A
Skin
23
Q
Microorganisms on the skin
A
Bacteria and yeast
24
Q
How does the skin prevent nonresident flora
A
- low skin pH
- dryness of skin
- skin produces lysozymes in sweat
25
What prevents microorganisms from getting to the back of the eye
Conjunctiva
26
How to tears prevent microorganisms from getting in the eye
Tears have lysozymes
27
What prevents microorganisms from living in the upper respiratory tract
Mucus (traps the microorganisms)
| Has lysozymes to trap and digest
28
What do ciliated cells do in the upper respiratory tract
Clean, moisten and warm
29
How do the lungs prevent microorganisms
Macrophages in the alveoli (alveolar macrophages)
30
What does saliva do to get rid of microorganisms
Mechanically flushes microorganisms to the stomach to be destroyed by acid
31
How is the growth of microorganisms prevented on the walls of the mouth
Desquamation of the epithelial cells
32
What microorganisms are on the teeth
Before they grow: aerobs and faculative
| After they grow: gram positive aerobs
33
Streptococcus mutans
Produce glucans in the presence of sugar (break down the enamel of the teeth)
34
Why doesnt the stomach have many microorganisms
The HCl
35
Microorganisms of the duodenum
Gram positive cocci and basilli
36
Microorganisms of the jujenum
- lactobacili
- entecococci
- candida
- cory.....
37
Microorganisms of the ilium
Anaerobs and faculative
38
How does the large intestine prevent microorganisms
- Mucus traps
- desquamation caused by movement of fecal matter
- peristalsis/hastral churning to keep the microorganisms moving through
39
What percentage of the microorganisms of the large intestines are anaerobs and faculative
Anaerobs: 99
Faculative: 1
40
`What influences the normal flora of the intestines
- antibiotics
- stress
- starvation
- diet
- bile acid
41
What parts of the urinary system should there be no microorganisms
Kidney
Ureter
Bladder
42
Where in the urethra is there microorganisms
Lower urethra (none in the upper part)
43
Pathogenicity
Capability of microorganisms to cause disease
44
Virulence
Degree to which the microorganism could cause disease
45
Virulence factors
Characteristics exhibited by microorganisms that make them more pathogenic (EX: capsule)
46
What must a pathogen do for disease to occur
1. Enter the host
2. Multiply. reproduction
3. Resist host's defenses
4. Damage tissues
47
Virulence factors (list)
- Toxins
- Extracellular enzymes
- Cellular factors
48
Toxins
Cause tissue damage
| Types: Endotoxins and exotoxins
49
Endotoxins
Produced in the microorganisms Retained in the microorganisms. Less toxic than exotoxins. Cause fever. Lipopolysaccharides. Gram -
50
Exotoxins
Released into the blood and are tissue specific. Gram positive and gram negative. Usually proteins
51
Types of exotoxins
Botulism and tetanus
52
Extracellular enzymes
Help microorganism to penetrate tissue (breaks down skin to get in)
53
Cellular factors
- Capsule: without a capsule, they lose their ability to cause disease
- Pili: suction cups/finger-like projections. Adhere to your cells
54
Factors that affect resistance
1. Stress
2. Age
3. Health
4. Nutrition
5. Hygene
6. Environment
7. Genetics
55
Defense mechanisms of the skin and mucus membranes
- Mechanical barrier (wall)
- Skin is dry, low pH, produces inhibitory substances
- Mucus traps microorganisms, does does the cilia of the mucus
56
Chemical secretions (defense mechanisms)
- Lysozymes
- Sebum
- Cerumen
- Gastric juices
- Transferin
57
Lysozymes
Digest the cell wall and membrane of microorganisms
58
Sebum
Oil produced by the sebacious glands. Prevents the skin from cracking
59
Cerumen
Earwax. Prevents microorganisms from getting into the ear
60
Gastric juices
Really low pH that microorganisms dont like
61
Transferin
Picks up free iron from dead RBC so the microorganisms cant get it
62
Defense mechanisms (list)
- skin and mucus membranes
- chemical secretions
- fever
- natural killer cells
63
How is a fever caused
- Endotoxins: affect the temperature regulating nuclei in the hypothalamus
- Endogenous pyrogens: Produced by the body after engulfing microorganisms. Go up to the hypothalamus and mess up heating mechanisms
- INcreased metabolic heat production: Vasodilation, decreased appetite, proteins break down (N is stripped from NH2)
64
What is the job of Natural Killer cells
Type of WBC
| Target the virus infected cells and tumor cells. Attaches to the cell, releases enzymes to destroy it
65
What is a chemical mediator and types
Any chemical that plays a role in defense mechanisms of the body
1. Plasma proteins
2. Cytokines
3. Chemotaxins
4. Opsonins
5. Chemical mediators secreted by mast cells
66
What are chemical mediators usually
Proteins or plasma proteins
67
How do plasma proteins travel
Circulate in the blood
68
Types of plasma proteins
- Antibodies
- Complement proteins
- Kinins
- Clotting factors
69
Antibodies
Immune response
70
Complement proteins
Fight off infection with cascade
71
Complement protein cascade to fight infection
C3B causes opsonization
72
What is opsonization
Makes connection through the capsule to kill bacteria
73
MAC
Complement protein complex that attacks by punching holes in the membrane and causes cytolysis
74
Kinins
Inflammation. Kininogen to kinin
75
Clotting factors
Fibrinogen to firbin
76
Cytokines
Chemicals secreted by WBC (lymphocytes, monocytes, macrophages) that regulate cells in defense mechanisms and act locally
77
Types of cytokines
1. Interleukens
2. Interferon
3. Tumor nucrosis factor
4. Lymphotoxins
5. Proforins
6. Macrophage migration inhibiting factor
78
Interleukens
Turn on the immune response
79
Interferons
Produced by cell infected by a virus. Attaches to a neighboring cell to prevent the virus from getting in
80
Tumor nucrosis factor
Kills sensitized tumor cell. Can activate WBC during inflammation
81
Lymphotoxins
Fragment DNA of the microorganism
82
Proforins
Perforates the microorganism. It floods and lyses
83
Macrophage migration inhibiting factor
Released so macrophages stay at the site of inflammation
84
Chemotaxins
Attract macrophages to the sit of inflammation
85
Opsonins
Enhance phagocytosis by coating microorganism to antibody can attach to it
86
Chemical mediators secreted by mast cells
1. Histamine
2. Leukotrienes
3. Prostaglandins
87
Histamine
Vasodilation of arterioles, increased capillary permeability
88
Leukotrines
Same as histamines. Also attract phagocytes
89
Prostagladins
Intensify effects of histamine and kinins
90
Is phagocytosis specific
No
91
Phagocytosis
Engulf and destroy microogranisms
92
Types of phagocytes
Granulocytes and Macrophages
93
Types of granulocytes
- Neutrophils
- Eosinophils
- Monocytes
94
Neutrophils
WBC that do most phagocytosis. First to arrive at the sit of infection
95
Eosinophils
Response to allergies, parasitic worms
96
Monocytes
Immature macrophages. Go to the infection site and mature
97
Types of macrophages
Wandering and fixed
98
Wandering macrophages
Travel through the blood until they are called
99
Fixed macrophages
In certain parts of the body
100
Skin fixed macrophages
Histeocytes
101
Spleen fixed macrophages
Splinic macrophages
102
Brain fixed macrophages
Microglial cells (CHECK)
103
Liver fixed macrophages
Kupffer cells (CHECK)
104
Lungs fixed macrophages
Alveolar macrophage
105
Kidney fixed macrophages
Mesangeal macrophages
106
Bone fixed macrophages
Macrophage
107
Phagocytosis sequence of events
1. Adherence: contact between phagocyte and bacteria (need opsonization if there is a capsule)
2. Ingestion (endocytosis) with pseudopods
3. Phagosome (name for bacteria that was engulfed)
4. Phagolysosome (lysosome fuses with phagosome to break it down)
5. Exocytosis
108
Is inflammation specific
No
109
Inflammation
Local response to tissue damage
110
Inflammation steps
1. Bacteria enter, multiply and cause damage
2. Mast cells of connective tissue release histamine (also cause release of prostagladins and leukotrienes)
3. Vasodilation of arterioles
4. Increased capillary permeability to plasma proteins (space between endothelial cells gets larger so plasma proteins can enter)
5. Chemotaxis of neutrophils (attraction of neutrophils to the area of damage. Leave blood by diapedesis. Destroy microorganisms)
6. Activation of complement system (C3B and MAC)
7. Kill microorganism
8. Repair tissue
111
MAC complex
C5,6,7,8,9
112
Inflammation symptoms
Redness, pain, heat and swelling
113
What causes the pain of inflammation
Kinins or a chemical from the microorganism
114
What causes the swelling of inflammation
Increased capillary permeability
115
Is the immune response specific
Yes
116
What must the immune response be/have
- Specificity
- Memory
- Body has to recognize self vs nonself
117
Humoral immunity
Antibody mediated
118
Cellular immunity
Cell mediated
119
Cells of humoral immunity
B and T lymphocytes
120
B lymphocytes
Differentiate from stem cells of bone marrow (mature when they leave). Migrate to lymphatic tissues and stay as resting inactive B cells in the mucus membranes
121
T lymphocytes
Differentiate from the stem cells of bone marrow (leave as immature T cell)
122
Where do T lymphocytes mature
Thymus gland
123
How do T lymphocytes mature
They pick up a protein (CD4 or CD8)
124
Subsets of T lymphocytes
Helper T cell (CD4), Cytotoxic T/Killer T (CD8), Suppressor T (CD4)
125
Where do mature T cells migrate to
Lymph nodes and spleen. Stay inactive until turned on
126
Major histocompatability complex (MHC)
Found on every cell with a nucelus. Recognizes self from nonself
127
How does a T cell turn on
T cell needs an antigen presenting cell with MHC. When MHC picks up an antigen, the T cell realizes the antigen presenting cell is no longer self and turns on
128
Antigen presenting cells
1. Macrophages
2. Dendrticic
3. B cells
129
Types of dendritic cells
- Langerhans (epidermis of skin)
- Follicular (lymph node and spleen)
- Interdigitating (lymph node and spleen where T cells are found)
130
Where are antigen presenting cells found
1. Epidermis of skin
2. Difuse lymphatic tissue
3. Lymph nodes
4. Spleen
131
Antigen
Any substance that the body recognizes as foreign
132
Endogenous
Antigens that originate inside the body. Cytotoxic T cells respond
133
Endogenous example
Virus gets in and infects cell. Cell becomes an antigen. Also cancer cells
134
Exogenous
Antigens that originate outside the body
135
Exogenous examples
Bacteria, fungus, yeast etc.
136
Antigen receptor
Protein on surface of T or B cell
137
Immunogenicity
Ability to provoke immune response
138
Antigenic determinant (epitope)
Site on antigen where T cells or antibodies bind. Makes it specific, each has a different epitope. Body make antibody specific for this spot
139
Haptan (partial antigen)
Cant cause immune response unless it combines with a body protein
140
What happens to complement 3 when it is activated
It splits (3A and 3B)
141
C3B
Opsonization, makes adherence
142
C3A
Increased vasodilation, acts like histamine
143
Function of complement proteins
- Inflammation
- phagocytosis
- cytolysis (MAC)
144
What can produce interferons
Helper T cells, macrophages, killer T cells, NK cells, and fibroblasts (must be infected by a virus)
145
Type 1 interferon
Suppresses tumor formation and prevents it from spreading
146
Type 2 interferon
Activates neutrophils and macrophages
147
Structure of antibodies
Proteins. Combines with antigenic determinant that triggered its production
148
Heavy chains
Identical. 450 amino acids
149
Light chains
Identical. 200 amino acids
150
How are chains attached
Disulfide bonds
151
Where is the antigen binding site
At the tip of the heavy chains in the constant region (bottom half)
152
What is the purpose of the antigen binding site
Makes antibody specific
153
What is the same for each antibody of a class
Constant chain
154
What is different for each antigen
Variable region
155
Mechanisms of antibodies
- Activation of complement system
| - Neutralization caused by antibody-antigen complex
156
Antibody classes
```
IgG
IgA
IgM
IgD
IgE
```
157
What percent of antibodies is IgG
75
158
IgG structure
Y (monomer)
159
Unique feature of IgG
Only type that crosses the placenta
160
Where is IgG found
Blood, lymph, and intestines
161
Job of IgG
Protects against bacteria and viruses by triggering the complement system, phagocytosis and neutralizing toxins
162
Percent of IgA
15
163
IgA structure
Monomer and dimer (2 Y's together)
164
Where is IgA found
Tears, saliva, mucus, breast milk, blood, lymph, GI secretions
165
IgA job
Provides localized protection on mucus membranes
166
Percent of IgM
5-10
167
IgM structure
Pentomer (5 Y's) or monomer on the surface of B cells
168
Where is IgM found
Blood, lymph, surface of B cells as antigen receptor
169
Job of IgM
Causes cytolysis of microorganisms , can be antigen receptor
170
Percent of IgD
Less than 1%
171
IgD structure
Monomer
172
Where is IgD found
Blood, lymph, surface of B cells as antigen receptor
173
Job of IgD
Activates B cells to make more antibodies
174
Percent of IgE
Less than 0.1%
175
IgE structure
Monomer
176
Where is IgE found
On mast cells and basophils
177
Job of IgE
Causes allergic response (allergies)
178
What is the first antibody class secreted after initial exposure to an antigen
IgM
179
What is antibody mediated immunity effective against
Extracellular pathogens (bacteria) and antigens dissolved in body fluids (toxins and viruses)
180
Antibody mediated immunity process
1. B cell recognizes antigen as foreign. Turns on and starts to divide (plasma cells)
2. Plasma cell produces antibodies that attach to antigen. Form antibody-antigen complex. Antigen is destroyed
3. Memory B sticks around until the antigen enters again and turns on
181
How does a B cell divide
Two plasma cells and a memory cell
182
Functions of antibody mediated immunity
1. Activates complement system
2, phagocytosis
3. Links toxins together (not deadly when linked)
183
What is cell mediated immunity effective against
Intracellular pathogens (fungi, protozoa, viruses), cancer cells, tissue transplants
184
Process of cell mediated immunity
- Helper T cell cant recognize antigen as foreign. Needs antigen presenting cell
- Turns on when it sees non self (something attached to MHC)
- Tells Killer T cell (cytotoxic T cell) to turn on and kill the antigen
- Tells B cells to produce antibodies (costimulaiton)
- Memory T cells stick around for next time
185
What does the cytotoxic T cell (killer T) cause
- Cytolysis
- DNA fragmentation
- Phagocytosis
186
Cytolysis
Release of perforin (perferates cell membrane of the microorganism). Cell gets big and explodes
187
DNA fragmentation
Lymphotoxin shreds DNA
188
What helps cause phagocytosis
Perforins and opsonins
189
What shuts down the immune response
Suppressor T cells
190
Naturally aquired active immunity
B and T cells activated
Antibodies and memory cells produces (active)
You got sick (natural)
191
Artificially acquired active immunity
Injection (artifically)
| Memory cells and antibodies produced (active)
192
Naturally acquired passive immunity
IgG from mother to fetus, or IgA through breast milk (naturally)
Fetus didnt make antibodies, mother did (passive)
193
Artifically acquired passive immunity
```
Immunoglobulin injections (artificially)
Antibodies not made by the body but are circulating (passive)
```
194
Lag phase
Time passes, growth rate=0
- no increase in cell numbers. Individual cells increase in size. Cells are synthesizing what they need, making enzymes and adapting to the environment
195
Log phase
Growth rate is max and constant. Most efficient phase
196
Stationary phase
Growth rate=0, waste products build up and nutrients are depleted. Some cells die but some are reproducing so it remains balanced
197
Death phase
Growth rate is negative. Waste is accumulated, nutrients depleted. Death is accelerated
198
Senescent population
What you are left with after the death phase. Eventually they will use what is left of the nutrients and die off
